The Origin of Biological Information, Part 3: CSI on Steroids

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April 7, 2011 Tags: Design

Today's entry was written by Dennis Venema. You can read more about what we believe here.

The Origin of Biological Information, Part 3: CSI on Steroids
If your heart is right, then every creature is a mirror of life to you and a book of holy learning, for there is no creature - no matter how tiny or how lowly - that does not reveal God’s goodness.

Thomas a Kempis - Of the Imitation of Christ (c.1420)

In part 2 of this series, we explored how the Long Term Evolution Experiment (LTEE) performed by the Lenski research group on E. Coli, demonstrates some key features of how biological “complex, specified information” (i.e. “CSI” as the ID movement terms it) arises through mutation and natural selection. To briefly recap, we noted that:

  1. CSI does not need to arise all at once, but can arise piecemeal through independent mutation events.

  2. Separate mutations that later combine to form CSI do not need to confer a specific advantage on their own. In other words, mutations that are “neutral” with respect to the survival of the organism can later be co-opted into CSI that does have a distinct survival advantage.

  3. Neutral mutations may open up new future paths. In the LTEE, the brand-new ability of one bacterial population to use citrate as a food source required that a neutral mutation appear several thousand generations before it combined with other mutations to provide the CSI for using citrate.

  4. When CSI arises, it can be pretty poor at the beginning. Nascent CSI, though poor, provides a survival advantage because it is the “best game in town” at that time. Further mutation in, and natural selection on, the offspring of the original CSI-holder quickly refine the nascent information into ever-more “specified” CSI.

And, as we noted at the close of the first post in this series, understanding how natural processes create information is in no way a threat to God’s ordaining and sustaining of creation. Rather, it is an opportunity to explore some of the mechanisms by which He does so.

With these important principles in mind, we are ready to examine a second fascinating case of a novel function arising through mutation and selection: the evolutionary history of steroid hormones and their protein receptors in vertebrates.

Experimental Evolution as Textual Criticism

The elegant work by the Lenski group has one very distinct advantage that other researchers surely envy: when new structures and functions arise in the experiment, a trip to the freezer is all that is needed to resurrect and examine the relevant ancestors. For researchers who study other organisms less amenable to laboratory experimentation, or for evolutionary transitions that happened deep in the past, other methods are needed. One approach to this type of problem is to “resurrect” ancient proteins in the lab in order to study their properties.

Bringing an ancient gene back to life starts with determining what its DNA sequence was, (and thereby determining the sequence of amino acids that made its functional protein product). While researchers don’t have direct access to ancient DNA, we have the next best thing: many modern examples of genes copied from the ancestral one.

For those who are familiar with textual criticism, the principles are very similar. Textual criticism is the process of recovering the words of an ancient manuscript by comparing several very similar, but still imperfect, copies. In general, as more copies agree on a certain wording, the more likely it is that the original had that wording. Also, the more widespread and older a certain wording is, the more likely it is original. Groups of manuscripts that have similar copying errors or other variations can be grouped together as more closely related, and so on. Given enough manuscripts, it is possible to recreate a copy of an ancient text with a very high degree of accuracy. As Christians, we benefit from this type of analysis daily when we read the Bible: though no two Greek manuscripts of the New Testament are exactly alike, scholars have used these methods to recover the original text with a very high degree of confidence.

And so too, for ancient gene sequences. Consider a hypothetical amino acid sequence in six modern organisms:

Though none of the modern sequences are identical, it is easy to see that there is a “consensus” at each of the 12 amino acid positions. This consensus sequence is very likely to be the ancestral sequence: explaining the pattern in any other way requires many more changes, with many changes occurring in parallel after species separate.

Once the researchers determine the correct ancestral amino acid sequence, it’s a relatively small matter to engineer a DNA sequence that encodes it and give it to cells to make into protein. This protein can then be tested to see how it functions compared to the modern sequence.

What makes this type of analysis even more interesting is that sometimes related genes acquire new functions. In cases like these, bringing the ancestral gene back to life in the lab allows researchers to not only test its properties, but to test hypotheses about what the specific amino acid changes were that changed the protein’s function over time:

The laboratory of Joseph Thornton at the University of Oregon has used this method (with great success) to determine how certain hormone / protein receptor complexes arose during vertebrate evolution. Hormones are small molecules that act as signals by binding to a protein target, called a receptor. The receptor / hormone pair then goes on to effect a change in the target cell by regulating other genes.

In vertebrates, two hormone – receptor pairs were of interest to the Thornton group: the mineralocorticoid receptor (MR), which binds a steroid hormone called aldosterone, and the glucocorticoid receptor (GR), which binds a second steroid hormone called cortisol (see diagram above). Cortisol can also activate MRs, but an enzyme that breaks down cortisol is present in tissues where MR is used so cortisol cannot accumulate. Aldosterone, on the other hand, cannot activate GR – it is specific to its binding partner MR. Even though these two hormone / receptor pairs regulate different processes in modern organisms, the two receptors are the result of an ancient gene duplication that occurred early in vertebrate evolution, around 450 MYA (million years ago). As time has gone by, the derivatives of the original gene have picked up distinct binding partners and physiological roles. Thornton and colleagues wanted to tease out the details of these important changes.

They started out by determining the ancestral sequence of the original receptor gene, prior to the duplication, and recreating it in the lab. When they tested this lab-designed protein, they found that it, like modern MRs, (but not GR’s)could bind either cortisol or aldosterone indicating that the ancestral protein must have been able to bind both. This result suggested that somewhere along the line the GR lost its ability to bind aldosterone and became specific to cortisol. This is interesting, because at the time the ancestral receptor was present, aldosterone didn’t exist. Aldosterone is a relative newcomer on the scene: it is present only in four-limbed vertebrates (tetrapods), which arose around 390 MYA. So, the ancestral receptor present prior to 450 MYA already had the ability to bind a hormone that wouldn’t evolve for tens of millions of years. Of course, the ancestral receptor “didn’t mind” – it had its own binding partner - a steroid hormone closely related to cortisol and aldosterone. It wasn’t sitting around doing nothing in the meantime.

This finding strongly suggested that the reason aldosterone binds only to MRs is because modern GRs, in contrast to the ancestral protein, have lost the ability to bind it. By comparing the amino acid differences between MRs and GRs, the Thornton group was able to test different combinations to see what the key changes likely were. They also did the (difficult) work of determining the precise new shape of the receptor for each of the changes that had an effect. All in all, it is an impressive body of scientific work.

Through these techniques, the Thornton group demonstrated that the loss of aldosterone sensitivity in GR occurred in a series of mutational steps that progressively remodeled the portion of the GR that binds the hormone molecule:

  1. First, a mutation occurred that altered one of the amino acids near the hormone binding site. This change had no effect on its own (it was a neutral mutation).

  2. Second, a change in an amino acid outside the binding pocket bent one side of the binding site into a new shape. Now the amino acid from the first neutral mutation in step #1 was thrust up against the hormone binding site. This amino acid can interact appropriately with cortisol, but not very well with aldosterone. The receptor was now strongly biased towards cortisol.

  3. Later, several more mutations accrue that “tune” the receptor to its new specificity. Some of the mutations are neutral at first (like step #1) and then combine with later mutations to refine the receptor into its modern cortisol-specific role.

As the GR and MR lineages were becoming functionally distinct, other changes in other genes accumulated that refined their ability to regulate different processes (such as the enzyme that breaks down cortisol where MR is present, or the target genes that the two hormones regulate). While many of those details remain to be worked out, this work is an elegant demonstration of how a new function arose: gene duplication; sequence divergence with a neutral mutation that opened up a new possible trajectory; a second mutation that altered function in one of the gene copies; further mutations that refined this nascent difference; and the final result of new structures and functions that act as key regulators of important physiological processes in tetrapods, including humans.

In other words, new CSI.

Over and against these lines of evidence, however, the Intelligent Design Movement claims that such novelty is inaccessible to random mutation and natural selection. Rather, they claim that functional protein shapes are incredibly rare and therefore so isolated from each other that random mutation and natural selection cannot bridge the vast gulfs between them. Though Thornton’s work (and the work of Lenski that we examined previously) refutes this claim with detailed, concrete examples, new comparative genomics tools have addressed this issue with greater power and breadth than ever before. In the next post in this series, we’ll explore the question: are these examples rare, isolated cases, or indicative of a wider pattern?

Further reading:

Harms, M.J. and Thornton, J.W. (2010). Analyzing protein structure and function using ancestral gene reconstruction. Current Opinion in Structural Biology 20: 360-366.

Bridgham, J.T., Carrol, S.M., and Thornton, J.W. (2006). Evolution of hormone-receptor complexity by molecular exploitation. Science 312: 97-100.

Thornton, J.W. (2004). Resurrecting ancient genes: experimental analysis of extinct molecules. Nature Reviews Genetics 5: 366-375.


Dennis Venema is Fellow of Biology for The BioLogos Foundation and associate professor of biology at Trinity Western University in Langley, British Columbia. His research is focused on the genetics of pattern formation and signalling.

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Ashe - #57375

April 8th 2011

I would think it would be discarded, but I can’t speak for Mike. Also,
the data that I’m aware of about Dicty was out a few weeks ago, long
after Mike’s hypothesis regarding beta-catenin.
http://designmatrix.wordpress.com/2010/12/29/nudging-beta-catenins-to-emerge/

Dicty
has unicellular and multicellular phases of its life cyle. It’s
phylogeny and this data suggests that there is an evolutionary
relationship between epithilial tissue in this critter and in animals.


John - #57383

April 8th 2011

“I would think it would be discarded, but I can’t speak for Mike.”

Why the passive voice, and why would we have to ask Mike? The question is, would YOU discard it?

“Also, the data that I’m aware of about Dicty was out a few weeks ago, long after Mike’s hypothesis regarding beta-catenin.”


Mike doesn’t have a hypothesis, and the Dicty genome sequence was completed in 2005. Mike is trying to pretend that unicellular organisms don’t respond to signals from other cells, i.e. pretending that signalling pathways are unique to multicellular organisms, and you are buying his deception. 

“Dicty has unicellular and multicellular phases of its life cyle.”

Yes, I know. I’ve published in the Dicty field and have been reentering it slightly during the last few weeks. Nothing Mike wrote in that post presents a testable, falsifiable hypothesis.

“It’s phylogeny and this data suggests that there is an evolutionary 
relationship between epithilial tissue in this critter and in animals.”

And how does that suggest front-loading? Try to avoid referring to Mike, as doing so prevents you from engaging your own brain.

Ashe - #57384

April 8th 2011

lol John that post makes no sense. The data I’m pointing to is not just sequences and not just about how signaling cells. The data is showing specifically that the structure in Dicty is very much like the structure in animal cells, which is expected from Mike’s hypothesis. There is no deception, it’s only in your own head. I’ll wait until you have an actual response with some substance rather than insults before responding to you again.


Ashe - #57403

April 8th 2011

John, nothing that you’ve written in this post has any relevance whatsoever. If you think it does, quote Mike’s actual essay and show it. Also, you claimed to be published in the Dicty, field. Reference? 


Bilbo - #57408

April 8th 2011

Dennis:  “I’d be interested in your reasoning as to why this isn’t a challenge to
Behe.”

And I would be interested in your reasoning as to why this is a challenge to Behe.

Meanwhile, Behe’s reasoning can be found here: 

http://www.discovery.org/a/3415

But again I agree that this seems to be a challenge to Axe.


Chris Massey - #57411

April 8th 2011

Dennis,


Do you think you could review the link that Bilbo has provided? Behe seems to have a very different take on the significance of the Bridgham paper at least. I’d be interested in your response.

John - #57413

April 8th 2011

Ashe,If you truly believe that it has no relevance, why not answer my question and make a fool of me: 


Why wouldn’t structures that mediate communication between cells in a multicellular state be very much like structures that mediate communication between cells in a single-cell state?

I predict that you won’t, and saying that my question has no relevance whatsoever is a far cry from demonstrating that it has no relevance.

There’s nothing about multicellularity that represents any great leap in complexity. That’s the deception that Mike is selling.

Ashe - #57417

April 8th 2011

“Why wouldn’t structures that mediate communication between cells in a
multicellular state be very much like structures that mediate
communication between cells in a single-cell state?


This is why I asked you to quote Mike. Where did Mike say that structures that mediate communication between cells in a multicellular state are completely different from structures that mediate communication between cells in a single state? You won’t find that claim anywhere. It’s the discovery of these same structures doing pretty much the same thing in ancient organisms that is interesting. And the fact that it may even be older.

Going back to the relevance of my discussion, the fact that Dicty does epithelial structures very much like animals lead researchers to say “Thus, the organizational principles of metazoan multicellularity may be more ancient than previously recognized”

By the way are you going to answer my question? I think it’s important with regard to this back and forth about deception.



John - #57775

April 12th 2011

Ashe:
“This is why I asked you to quote Mike.”

But I was quoting and challenging you:
“The data is showing specifically that the structure in Dicty is very much like the structure in animal cells, which is expected from Mike’s hypothesis.”

“Where did Mike say that structures that mediate communication between cells in a multicellular state are completely different from structures that mediate communication between cells in a single state?”

That was quite the rhetorical move, Ashe. Let’s go back to quoting Mike:
“I was able to track down some papers which uncovered evidence for the existence of various adherens junctions proteins in unicellular organisms. Well, a few days ago, I had the time to probe databases with sequence from human genes in search of homologs for adherens junction proteins in unicellular organisms.”

And what happens when one probes the human database with the alleged Dicty adherens junction protein homolog? It’s very easy to do, but I predict you’ll find an excuse for not doing it.

“You won’t find that claim anywhere. It’s the discovery of these same structures doing pretty much the same thing in ancient organisms that is interesting. And the fact that it may even be older.”

But what is the alleged “same thing” that they are doing, exactly? That’s where Mike is fooling himself and fooling you.

“By the way are you going to answer my question? I think it’s important with regard to this back and forth about deception.”


Which question? 

Ashe - #57782

April 12th 2011

John, you made some claims about Mike’s assertions that Mike never made. You don’t quote Mike, precisely because he never made them. 


There’s no deception here, it’s all in your head, I of course was referring to the three things that ddicty is doing that is pretty much the same as it is being done in animal cells. I discuss it in comment #57354

You asked:
Which question? 

You claimed:
I’ve published in the Dicty field and have been reentering it slightly during the last few weeks. “

Reference? I expect that you won’t answer this question. 


John - #57954

April 13th 2011

Ashe,


Take human beta-catenin and BLAST it against the Volvox genome. Then take the top hit from Volvox and BLAST it against the human genome. This takes 5 minutes. 

You don’t get human beta-catenin, you get:

emb|CAB66793.2| hypothetical protein [Homo sapiens]Length=537
GENE ID: 55130 ARMC4 | armadillo repeat containing 4 [Homo sapiens]

IOW, Mike’s claims about function have no evidentiary basis. He’s conflating the presence of Arm repeats with beta-catenin-like function (i.e., conflating a widespread repeat with an ortholog), fooling himself and you.

As for your question, I’m not making any arguments from authority, just telling you that it’s unnecessary for you to tell me how Dicty works.

Ashe - #57958

April 13th 2011

John wrote:
IOW, Mike’s claims about function have no evidentiary basis

No John, that is simply not true. The formation of epithelial tissue requires two proteins in dicty, beta-catenin and alpha-catenin, that are also necessary for correct organization of animal epithelia. The beta-catenin in dicty is thought to be a homolog of human beta-catenin. So Mike Gene’s claims about function have evidentiary basis. 


Also,since even a protozoa, choanoflagelata has a cadherin gene, I can believe that Volvox has beta catenin.

John - #57964

April 13th 2011

Ashe:
“Also,since even a protozoa, choanoflagelata has a cadherin gene, I can believe that Volvox has beta catenin.”

The actual evidence, as I pointed out in my post, clearly shows that Volvox does not have a beta catenin, it just has an Arm repeat-containing protein. 

If the Volvox protein was homologous to beta-catenin, blasting in reverse should have pulled out human beta-catenin at the very top of the list. It doesn’t, so the following statement from Mike:

“The beta-catenins are found in green algae (Volvox), indicting that they existed in the last common ancestor of green algae/plants and animals.”

...has no evidentiary support. The problem is that Mike quit when he found what he wanted to find, and didn’t entertain the possibility that he was wrong.

I am enjoying your Nigel Tufnel impression, though.

Ashe - #57970

April 13th 2011

If the Volvox protein was homologous to beta-catenin, blasting in reverse should have pulled out human beta-catenin at the very top of the list. It doesn’t, so the following statement from Mike


So you’re saying that any known homologous proteins wouldn’t exhibit this type of result. Is that right?




John - #57974

April 13th 2011

Correct. Mike allowed himself to be fooled by the repeats.


John - #57975

April 13th 2011

Let me add to that by saying that even if they did give the right result, that still wouldn’t be sufficient evidence for claiming that their functions are homologous. But it is necessary.


Ashe - #57976

April 13th 2011

Well Mike Gene didn’t say it matter of factly, he said it was a testable hypothesis that Volvox has a beta-catenin, and that it was a putative homolog. I’m pretty confident that Volvox has a beta-catenin. Regardless I’ll take a look at the issue. Doesn’t really change the overall gist of my discussion though. 



John - #57977

April 13th 2011

“Well Mike Gene didn’t say it matter of factly, he said it was a testable hypothesis that Volvox has a beta-catenin, and that it was a putative homolog.”


More wishful thinking.

No qualifications here:

The beta-catenins are found in green algae (Volvox), indicting that they existed in the last common ancestor of green algae/plants and animals.

Now, as I have shown, all the major components of these structures that are used to form multicellular organisms have homologs that exist in unicellular organisms. But the most interesting finding is the homolog for human beta-catenin in the green algae, Volvox carteri.


“I’m pretty confident that Volvox has a beta-catenin.”

Why? Because Mike said so without providing real evidence?

Ashe - #57979

April 13th 2011

You’re only pretending to have forgotten this:

“However, I do think your concern is indeed legitimate, as you may be right….However, right now, this is mostly a testable hypothesis.  What is needed are functional assays with this protein to seal the deal.”


John wrote:
Why? Because Mike said so without providing real evidence?

Because of all the similarities. 

John - #57983

April 13th 2011

“You’re only pretending to have forgotten this:”

No, I’m not ignoring Mike’s walking it back. That was after I pointed out the error, and Mike was still ignoring the important necessary/sufficient distinction.


I predict that neither Mike nor you are going to do “what is needed” in this case.

What’s interesting is that you persisted in claiming that Mike was right even after he had walked it back here.

Ashe - #57993

April 14th 2011

Once again, you’re just making things up. I didn’t “persist that Mike was right”, I’m simply expecting/predicting that beta-catenin is in Volvox. You know, that stuff about specifying stuff before the critical data is even available. You might want to  look into that. 


John - #58012

April 14th 2011

“ I’m simply expecting/predicting that beta-catenin is in Volvox. You know, that stuff about specifying stuff before the critical data is even available.”


What critical data, Ashe?

“You might want to  look into that.”

I did, you didn’t. The Volvox genome was sequenced 4 years ago, which would be the critical data. What empirical data are you predicting?

Ashe - #58017

April 14th 2011

I thought I was pretty clear, I’m predicting, in the absence of the critical data, that Volvox has a beta-catenin. Why do you bring up the fact that the Volvox genome was sequenced? To know to which extent this XP_002955847.1 protein can be related with beta-catenin at a functional level , what needs to be done is to analyze the conservation of some functional domains and perform functional experiments.There could very well be a beta-catenin like protein in Volvox, but recognizing that vs.
other Armadillo-repeat protein is of course tough, because the BLAST hits will often only pick up some of the Arm repeats.



Ashe - #58019

April 14th 2011

I did, you didn’t. 


I didn’t what John? What are you making up now? 

Jon Garvey - #58023

April 14th 2011

It’s not just me, then.


John - #58029

April 14th 2011

“I thought I was pretty clear, I’m predicting, in the absence of the critical data, that Volvox has a beta-catenin. Why do you bring up the fact that the Volvox genome was sequenced?”

Because those are the critical data.

“To know to which extent this XP_002955847.1 protein can be related with beta-catenin at a functional level, what needs to be done is to analyze the conservation of some functional domains and perform functional experiments.”

So why not do the former from the comfort of your armchair in less time than it takes to post a comment here? The termini that lack Arm repeats don’t pick up anything of significance. You and Mike are being fooled by labels.

“There could very well be a beta-catenin like protein in Volvox, but recognizing that vs. other Armadillo-repeat protein is of course tough, because the BLAST hits will often only pick up some of the Arm repeats.”

Uh, no, you’re completely wrong. The problem with Mike’s rush to judgment is that the BLAST only picked up the Arm repeats. They are found in many different proteins with many different functions. 


Does that suggest a major flaw in Behe’s claims about “CCCs”?

“I didn’t what John”

Look into it for yourself, Ashe. Your curiosity seems to have evaporated.

Ashe - #58032

April 14th 2011

Uh, no, you’re completely wrong. The problem with Mike’s rush to judgment is that the BLAST only picked up the Arm repeats. They are found in many different proteins with many different functions.


Um, how is what I said completely wrong when that was exactly my point? And I don’t really have a dog in the Volvox fight, I wouldn’t be surprised at all if beta-catenin isn’t found in Volvox. It’s just an interesting sideshow, and irrelevant to my discussion. 


John - #58036

April 14th 2011

Ashe:
“Um, how is what I said completely wrong when that was exactly my point?”

Ah, now I see what you are saying. 


Given your reluctance to accept that your prediction is false, it could just as easily be interpreted as you claiming that an insufficient number of the Arm repeats had been shown to be homologous.

“And I don’t really have a dog in the Volvox fight, I wouldn’t be surprised at all if beta-catenin isn’t found in Volvox.”

But there’s no reason for it to be a fight, you had predicted that it would be found, and you won’t accept that a necessary precondition isn’t there despite searching the whole genome.

“It’s just an interesting sideshow, and irrelevant to my discussion.”

But that’s my point! 

Frontloading is so vacuous that you can’t point to any condition that would falsify it. It doesn’t matter to you that Mike was wrong, even though when you thought that when he was right, it supported frontloading.

Ashe - #58039

April 14th 2011

So, can you quote me where I said that if Volvox has a beta-catenin it supports front-loading? I never said any such thing. I only talked about the findings in Dicty support front-loading. If those findings did not exist, that would be a problem with Mike’s hypothesis regarding epithilia.






John - #58075

April 15th 2011

Ashe:

So, can you quote me where I said that if Volvox has a beta-catenin it supports front-loading?”

“I thought I was pretty clear, I’m predicting, in the absence of the critical data, that Volvox has a beta-catenin.”


So you made this prediction independent of any frontloading hypothesis? If so, what hypothesis prompted it?

Ashe - #58078

April 15th 2011

The armadillo repeats but your point about the reciprocal hits is a good one. 


Mike Gene - #58082

April 15th 2011

Now that another work week is done, I have a little time to join in.  

John: The actual evidence, as I pointed out in my post, clearly shows that Volvox does not have a beta catenin, it just has an Arm repeat-containing protein.

My goodness.  When we last talked about this about four months ago, you did not adopt such an extreme position.  Back then, you noted, “I suspect that they are simply members of the ARM family.”  I respected that position and noted it as a legitimate cause for doubt, arguing that we needed functional data to resolve the issue.  But now you are
claiming real knowledge; that the evidence “clearly shows” that Volvox does NOT have a beta-catenin homolog.  Did you come up with some new data since then?  Just how were you able to rule this out, once and for all?  It looks like the same test to me:

If the Volvox protein was homologous to beta-catenin, blasting in reverse should have pulled out human beta-catenin at the very top of the list.

Not so fast.  As I told you back then, if you use the Aardvark sequence to probe the Volvox genome, the Volvox protein-in-question tops the list.  Use the Volvox protein to probe the Dictylostilium genome and Aardvark tops the list.  Given that Aardvark is a known homolog of beta-catenin, and has just been shown in interact with a newly discovered alpha-catenin homolog to help generate epithelial tissue that shows polarized secretion in slime molds, just precisely how does the probing of the human genome rule out the Volvox protein as being homologous to Aardvark, a known beta-catenin?  And if we use either Aardvark or the Volvox protein to probe the sponge genome, beta-catenin tops the list.  Just precisely how does the probing of the human genome rule out the Volvox protein as being homologous to the sponge beta-catenin?  

Better yet, I spent five minutes using the Aardvark sequence to probe the human genome.  According to your test, human beta catenin should be at the very top of the list because Aardvark is a known homolog of beta catenin.  But guess what?  No such luck.  The top two are a hypothetical protein and armadillo repeat-containing protein 6 isoform 2.  Human beta catenin comes in at  #14 on that list.  The Volvox protein better matches human beta-catenin than does Aardvark.

So according to your test, Dictylostilium does not have a beta catenin and Aardvark is just an Arm repeat-containing protein.

Now that leaves me with one of two choices.  Either the labs that have worked with this system have “fooled” themselves” into thinking that Aardvark is a beta-catenin homolog or your test can generate false negatives.  I opt for the latter explanation.  

So once again, I am not claiming that Volvox does indeed have a beta-catenin homolog, as it could very well be just an Arm repeat-containing protein.  It is simply a hypothesis supported by some evidence in need of more evidence to reach a conclusion.  You, on the other hand, have already delivered a conclusion – “The actual evidence, as I pointed out in my post, clearly shows that Volvox does not have a beta catenin, it just has an Arm repeat-containing protein.”  It looks to me like you have jumped to a conclusion.


John - #58085

April 15th 2011

John: The actual evidence, as I pointed out in my post, clearly shows that Volvox does not have a beta catenin, it just has an Arm repeat-containing protein. 

Mike: “...But now you are claiming real knowledge; that the evidence “clearly shows” that Volvox does NOT have a beta-catenin homolog.”


Anyone else notice the extra word that Mike slipped in to construct his straw man? I wrote “a beta-catenin,” and Mike claims I wrote “a beta-catenin homolog.

“Did you come up with some new data since then?”

Bill Weis did. Read parts B and C of the supplement from his lab’s Science paper:

www.sciencemag.org/content/suppl/2011/03/07/331.6022.1336.DC1/Dickinson-SOM.pdf

“Not so fast.  As I told you back then, if you use the Aardvark sequence to probe the Volvox genome, the Volvox protein-in-question tops the list.  Use the Volvox protein to probe the Dictylostilium genome and Aardvark tops the list.  Given that Aardvark is a known homolog of beta-catenin,…”

Of course it’s a homolog, Mike! But is is more homologous to beta-catenin or other homologous proteins with Arm repeats? Is it an outlier when you look at the nested hierarchy? If so, you can’t simply call it “a beta-catenin,” particularly if you can’t say whether it’s closer to beta than it is to alpha-catenin or plakophilin.

”... and has just been shown in interact with a newly discovered alpha-catenin homolog to help generate epithelial tissue that shows polarized secretion in slime molds,…”

But it does NOT function as a transcriptional coactivator, nor does it have the phosphorylation sites that regulate activity, and most important, nor is it required for epilthelial formation. 

”... just precisely how does the probing of the human genome rule out the Volvox protein as being homologous to Aardvark, a known beta-catenin?”

Aardvark isn’t a “known beta-catenin,” Mike, it’s a known beta-catenin homolog that differs in several biologically-important ways. Two very different things.

Ashe - #58088

April 15th 2011

I keep posting in the wrong thread.


John wrote:

nor is it required for epilthelial formation. 

Actually, beta-cateinin in Dicty is required for epithelial formation. Also, Aardvark has an alpha-catenin binding site, but fungal Arm repeat proteins like yeast Vac8 do not.  I think the presence of this site is diagnostic of a “true” beta-catenin, at least from the point of view of its role in epithelial structure.  

John - #58089

April 15th 2011

Ashe:

Actually, beta-cateinin in Dicty is required for epithelial formation.”

Actually, it appears that it was more wishful thinking than careful analysis, if you had bothered to read what I cited. Wishful thinking is a very strong drug, and careful scientists do things like double-blinding before analysis.

“Also, Aardvark has an alpha-catenin binding site, but fungal Arm repeat proteins like yeast Vac8 do not.”

Yes, but it lacks the signalling features of beta-catenin and it isn’t required for the formation of junctions. More importantly, it’s an outlier in the nested hierarchy to the group of beta-catenins plus plenty of non-beta-catenins.

“I think the presence of this site is diagnostic of a “true” beta-catenin, at least from the point of view of its role in epithelial structure.”

That’s nice, but since you can’t even be bothered to read up on the most recent data even when provided with a direct link, it’s safe to discount your opinion as wishful thinking.

Ashe - #58092

April 15th 2011

Actually, it appears that it was more wishful thinking than careful analysis, if you had bothered to read what I cited. Wishful thinking is a very strong drug, and careful scientists do things like double-blinding before analysis.”

Huh? You said Aardvark isn’t required for epthelial formation, the actual data and the paper state the exact opposite:

“Although D. discoideum lacks a cadherin homolog, we identify an α-catenin ortholog that binds a β-catenin–related protein. Both proteins are essential for formation of the epithelium, polarized protein secretion, and proper multicellular morphogenesis. ”

“both Ddα-catenin and Aardvark are required to organize and polarize the tip epithelium during culmination.”

“Yes, but it lacks the signalling features of beta-catenin”

Which signaling features? 

“More importantly, it’s an outlier in the nested hierarchy to the group of beta-catenins plus plenty of non-beta-catenins.”

What do you mean by that exactly? 


Ashe - #58093

April 15th 2011

Oh nevermind John, I just got what you’re saying. However, I don’t think your point is relevant. The claim isn’t that beta-catenin is an exact copy of metaozoan beta-cateinin. 


Ashe - #58094

April 15th 2011

That’s nice, but since you can’t even be bothered to read up on the most recent data even when provided with a direct link, it’s safe to discount your opinion as wishful thinking.


I just read this and I’m lost again, why don’t you think Aardvark is a “true” beta-catenin? Please be as specific as you can.  

John - #58098

April 15th 2011

C. Aardvark is not essential for formation of D. discoideum cell-cell junctions

Grimson and colleagues (S2) described actin-associated cell-cell junctions in the D. discoideum culminant that were reported to be absent in an Aardvark knockout strain. We confirmed the existence of these junctional structures in D. discoideum culminants, but we observed these structures Aardvark knockouts similar to wild-type (Fig. S16). Importantly, we used the same Aardvark knockout strain as Grimson et al., so our results cannot be explained by a difference in strain. We do not have an explanation for this discrepancy, but we note that we quantified these junctional structures by counting them in samples that were blinded prior to examination by TEM. No such quantitation was reported in previous studies (S2, S36).

This is what I mean by wishful thinking. This is why the pretense that science is about debate is such a pernicious lie—scientists are supposed to do the best they can to falsify their own hypotheses, and a primary method is blinding.


The actin-associated junctions in D. discoideum fruiting bodies were previously referred to as “adherens junctions” (S2, S36), but several lines of evidence indicate that these structures are not homologous to metazoan adherens junctions. First, the β-catenin-related protein Aardvark is not required for the formation of actin-associated junctions (Fig. S16). Second, although the Aardvark binding partner Ddα-catenin localizes to cell-cell contacts, it is not enriched adjacent to the stalk tube where these actin-associated junctions are found (Fig. 2c). Finally, D. discoideum does not have cadherin homologues, which are the primary transmembrane adhesion molecules found in metazoan adherens junctions (see materials and methods).

Ashe, your use of terms like “exact copy” and “true” only obfuscates. Nothing is an exact copy, which is why IDCreationists misrepresent the sequence evidence as mere similarity. 

The term you’re avoiding is “ortholog,” and that’s one of the main reasons why you and Mike are lost.


Ashe - #58099

April 15th 2011

This is my last post for tonight, I’m going to bed. But I don’t see how Aardvark not being essential for the cell-cell junctions means that it’s not required for epithelial formation or that it’s not a true beta-catenin, or how Aardvark not being essential for cell-cell junctions means I’m “wishful thinking”. I asked you to be more specific. 


Mike Gene - #58115

April 16th 2011

John: Anyone else notice the extra word that Mike slipped in to construct his straw man? I wrote “a beta-catenin,” and Mike claims I wrote “a beta-catenin homolog.

Okay, let’s deal with the semantics, as I was not trying to construct any straw man by slipping in any word.  You are the one who framed your claim as a choice between beta catenin and “just” an “Arm repeat-containing protein.”  In reality, there is middle ground between the two, middle ground that would be occupied by transitional states.  The question that interests me is whether this middle ground was already being traversed prior to the emergence of metazoa.   In other words, were preadaptations in play helping to facilitate the emergence of metazoa?  The alternative would have the initiation of these transitions occur concurrently with the evolution of metazoa as part of a vast co-evolutionary network under some broad selection pressure for the metazoan state.  

For a few years now, my front-loading perspective has led me to expect the former and I am thus encouraged to see the recent Science paper conclude:

In either case, our results identify unexpected similarities in tissue organization between two groups of distantly related organisms that were thought to have independently evolved multicellularity, and thus reveal molecular factors and organizational principles that may have contributed to the early evolution and diversification of animals.


And

Thus, the organizational principles of metazoan multicellularity may be more ancient than previously recognized, and the role of the catenins in cell polarity predates the evolution of Wnt signaling and classical cadherins.

Not exactly conclusions that should discourage me from viewing through the prism of front-loading.  

Look, we’re both supposed to be Christians, right?  Instead of pointing fingers, making accusations, and trying score points, let’s agree that we have a classic example of miscommunication here.  For it seems to me that you are under the mistaken impression that I am proposing the human beta catenin protein is floating about in the cytoplasm of Volvox.  For that is the claim that your 5 minute BLAST test would refute.  It’s not a test that falsifies a homologous relationship, as I showed with Aardvark. What I have been proposing is that this Volvox protein is a beta-catenin-like protein.  It’s a hypothesis - the middle ground of transitional states toward beta-catenins was already under way  before the emergence of metazoa.

Of course it’s a homolog, Mike! But is is more homologous to beta-catenin or other homologous proteins with Arm repeats? Is it an outlier when you look at the nested hierarchy? If so, you can’t simply call it “a beta-catenin,” particularly if you can’t say whether it’s closer to beta than it is to alpha-catenin or plakophilin.

Well, I told you back in December that I was a novice with trees when I made a tree that showed the Volvox protein to nest with human beta-catenin and Aardvark to the exclusion of those hypothetical human proteins.  Since I’m a novice with tree making, I’m not sure a negative or positive result would mean all that much.  Nevertheless, I’ll give it a try this summer (I’d love to do it this weekend, but several family chores are on the schedule). I’ll randomly choose a dozen proteins with Arm repeats and compare with the human, sponge, Dicty, and Volvox proteins and see what falls out.

But it does NOT function as a transcriptional coactivator, nor does it have the phosphorylation sites that regulate activity, and most important, nor is it required for epilthelial formation.

Yes, it does not behave exactly like a metazoan beta-catenin.  

Aardvark isn’t a “known beta-catenin,” Mike, it’s a known beta-catenin homolog that differs in several biologically-important ways. Two very different things.

Okay, it’s a known beta-catenin homolog that exists outside of, and thus prior to, metazoa.  With regard to the Volvox protein, the hypothesis is that the hypothetical protein I have raise has more similarities to Aardvark than the mere ability to stick to other proteins.  

Let’s also take another angle on all this and return to your claim that the Volvox protein is just an Arm repeat-containing protein.  Such proteins exist in all three domains – bacteria, archaea, and eukarya.  Yet does one domain make more extensive use of Arm repeat-containing proteins?


John - #58158

April 18th 2011

See page 5.


Mike Gene - #57429

April 8th 2011

Hi Dennis,

Perhaps Mike Gene may offer his thoughts on that.

First things first, as I suspect most people around here have mistaken views of front-loading.  For example, you write above, “In other words, new CSI.”  I fully agree.  So let’s make sure no one is working under the misconception that front-loading is somehow tied to the belief that CSI could not have evolved.  Any evidence for the design of evolution is not going to be found by trying to cast evolution as a failure.  Think of it as the good design vs. bad design argument.  Evolution itself is a good design and it is looking like a better and better design the more we understand it.  Yet most ID people try to cast evolution in the bad design light, as something that cannot do hardly anything of significance.  

One of the reasons proteins can mutate and adapt is because they are flexible - they’re not rigid structures.

Yes!  But this is not a side-point.  It’s one of the features of proteins that make them amazing design material.  

http://designmatrix.wordpress.com/2009/09/30/amazing-proteins/

Chris Massey writes, “The best antidote to Behe/Axe et al. is evidence of the creative power of random mutation and natural selection (plus neutral drift).”  Sure, but to what extent is that creative power of random mutation and natural selection indebted to protein biochemistry?  After all, what you outline above is a protein-dependent reality.  Without proteins, just how much creative power does random mutation and natural selection really have?  


To be fair to Mike, I’m pretty sure he doesn’t present his ideas as scientific - but he can speak for himself (I haven’t read his book).

Correct.  However, even though they may not be scientific, they are rational and are supported by evidence.  Anyway, if you are interested in the hypothesis of front-loading, take five minutes and read these:

http://designmatrix.wordpress.com/2010/05/19/nudge-2/
http://designmatrix.wordpress.com/2010/05/30/designing-evolution/

I see how the “front loading view of design” could be scientifically testable. That and the clear role of neutral mutations (in this example and in Lenski’s work) o goes against the idea.

How so?  Let me quote from my book:

“Front-loading does not allow for a prediction of specific outcomes, at a specific time and place, but does allow that specified outcomes can be made much more likely. A rough analogy to the concept of front-loading is the Las Vegas casino. As long as enough people gamble in the casino, it makes a profit. Yet the profits are derived by people playing games of chance. We cannot predict that a given casino will enjoy a specific profit at a specific time. But we can predict that the casino will profit, because the rules inherent in the games of chance favor the casino. In other words, it is the rules behind the games of chance that front-load profits for the casino.

Front-loading, by definition, is about designing the future through the present. It is about imposing some kind of constraint on evolution, or more simply put, it is using evolution to carry out design objectives. Since evolution would proceed outward from the originally designed cells, evolution may have been endowed with various sequences and structures to increase the odds that certain future states would be found through a random search stemming outwards from this front-loaded state. These sequences and structures
might act like the rules of the casino, where the initial design events may express themselves throughout their subsequent history, acting as the surrogates for the artificial selector.”



Mike Gene - #57431

April 8th 2011

I see there is a lot of talk about predictions around here.  So I’m curious.  Before they did a single experiment, did the Thornton group predict that the ancestral receptor protein would bind to both cortisol and aldosterone?


John - #57965

April 13th 2011

Why would they have done the experiment if the hypothesis hadn’t made the prediction?


Remember, Mike, useful hypotheses make unambiguous predictions. We don’t need to attribute them to people.

Alan Fox - #57437

April 8th 2011

...CSI could not have evolved.


Just for clarification, Mike, what do you mean by CSI?  Or are you using it, like Dennis “for the sake of argument”?

You quote yourself:

Front-loading does not allow for a prediction of specific outcomes, at a specific time and place, but does allow that specified outcomes can be made much more likely. A rough analogy to the concept of front-loading is the Las Vegas casino. As long as enough people gamble in the casino, it makes a profit. Yet the profits are derived by people playing games of chance. We cannot predict that a given casino will enjoy a specific profit at a specific time. But we can predict that the casino will profit, because the rules inherent in the games of chance favor the casino. In other words, it is the rules behind the games of chance that front-load profits for the casino.

So you say that what scientists might describe as stochastic events are only apparently so and the “Designer” or God can produce what appears to scientists as unguided evolution via random mutation and natural selection by “loading the dice”. I wonder, assuming this process would be invisible to any kind of observation or study, how you conclude this to be the case, other than a leap of faith?



R Hampton - #57439

April 8th 2011

Alan Fox,

So
you say that what scientists might describe as stochastic events are
only apparently so and the “Designer” or God can produce what appears to
scientists as unguided evolution via random mutation and natural
selection by “loading the dice”. I wonder, assuming this process would
be invisible to any kind of observation or study, how you conclude this
to be the case, other than a leap of faith?

It’s a matter of Faith and Reason, see my comment here:

http://biologos.org/blog/design-in-nature-part-4/#comment-57388


Mike Gene - #57441

April 8th 2011

Hi Alan,

Just for clarification, Mike, what do you mean by CSI?  Or are you using it, like Dennis “for the sake of argument”?

There is no “for sake of argument.”  I used it like Dennis did.   I explained this a  couple of years ago:

http://designmatrix.wordpress.com/2009/01/17/misunderstandings-about-front-loading/  

So you say that what scientists might describe as stochastic events are only apparently so and the “Designer” or God can produce what appears to scientists as unguided evolution via random mutation and natural selection by “loading the dice”.


No, I thought I was clear.  Truly stochastic events can be used to carry out objectives.  It depends on the context.  And front-loading is about setting the context (as explained in my essays on nudging evolution linked above).

I wonder, assuming this process would be invisible to any kind of observation or study, how you conclude this to be the case, other than a leap of faith?

It’s a matter of seeing the big picture.  There is no need to interpret all of evolution through a non-teleological filter.  If you prefer to view evolution as a purely non-teleological process, that is your choice and I respect it.  But I explore other neglected possibilities.  


nedbrek - #57448

April 8th 2011

Jon Garvey (57348) “Judging by the SETI program, not many planets in the neighbourhood have evolved radio transmitters yet. No doubt the Universe will be found to be teeming with intelligent life, but we’ll still be able to make a fortune selling them mobile phone franchises. Carl Sagan never predicted that.”

The true irony of SETI is that you have astronomers looking for signal among noise as a sign of intelligent design, sitting down the hall from biologists looking at signals which supposedly do not indicate intelligent design

The biggest problem for those who dream of a human galactic empire is that if the Earth truly is as old as we believe, and the universe is as flat as we believe, then the aliens should have already been here.  Probably not on the Earth (gravity wells are more trouble than they’re worth), but they would mine the asteroids.

The fact that we have asteroids indicates no aliens - or that no intelligent life ever leaves home (we’ll blow ourselves up).


alanfox - #57483

April 9th 2011

Sorry for not being clear, Mike. I was wondering if you understood anything by the term, CSI, as it seems impossible for anyone to give any kind of explanation or definition that means anything. As you used CSI in a sentence I was curious as to if you gave the term any credence.  It is no big deal, in any event. Your link doesn’t address CSI.


No, I thought I was clear.

A dangerous assumption when both Bilbo and I are around

Truly stochastic events can be used to carry out objectives.

How so? By definition, a stochastic event is not predictable (though I see that an apparently random series of chance occurrences  having the “dice loaded” is a way for non-theists and theists to dispense with arguments over intentionality in the scientific realm).





Jon Garvey - #57492

April 9th 2011

Alan, I don’t see the problem here. If I get people to write random letters on a folded sheet without knowing what’s already written, nonsense will result nearly always.

If I load the system with rules for the game of consequences, I ensure that the people write random sentences of a certain kind, and end up with a story every time - some of which may be funny, many less so. My system can tolerate spelling mistakes etc, but filters out more major errors.

A complex genetic code has good filters for random coding errors, but much higher tolerance for more “sophisticated” errors like reorganisation of genetic switches. So at the very least, it ensures that you get a litter of varied pups nearly every time, rather than 1 pup and 8 stiilbirths.

So the randomness is actually channeled by the code into potentially useful outcomes (wrt more adaptive offspring). “Objectives” is, of course, a teleological way of describing it - but no more invalid than describing amoeba’s “objective” as gaining food. It’s still a function of the living organism rather than mere accident.


alanfox - #57485

April 9th 2011

Nedbrek:


The true irony of SETI is that you have astronomers looking for signal among noise as a sign of intelligent design, sitting down the hall from biologists looking at signals which supposedly do not indicate intelligent design 

(Smiley noted but) this conflation between “design” as a characteristic of humans and other organism to some general mystical property does get a little tiresome. And as yet there are no anomalous signals to examine. The conclusion does not yet exist. First find a signal that is anomalous, as Jocelyn Bell did, then search for explanations. I think the  SETI project is a great idea, the more so because it is low-key. Look for evidence first and try to explain it when you have it.



Alan Fox - #57486

April 9th 2011

@ R Hampton #57439


So does the concept of “apparently” stochastic events help us avoid arguments over scientific interpretation of observed phenomena?

Dennis Venema - #57488

April 9th 2011

Hi Mike, where I said:


I see how the “front loading view of design” could be scientifically testable. That and the clear role of neutral mutations (in this example and in Lenski’s work) o goes against the idea

I meant to say I can’t see how….   rather changed my intended meaning there. 

I’ll try have a look at those links tomorrow. Thanks for contributing. 

Jon Garvey - #57499

April 9th 2011

It seems to me that a fair amount of untestable “front loading” is already inherent in evolution.

We have a universal genetic code able to synthesise a novel type of foldable chiral polypeptide which can facilitate complex chemistry at low temperatures at micro level, and on which the code itself depends for survival. Those proteins exist within a functioning cell which is self-sustaining and able to reproduce successfully for 3.5bn years.. We don’t know, and neither can we test, the origin of any of that.

Mike’s suggestion would appear to be small beer in comparison to what we already accept as axiomatic.


John - #57773

April 12th 2011

Jon Garvey wrote:
“Mike’s suggestion would appear to be small beer in comparison to what we already accept as axiomatic.”

I don’t know who you’re talking about, Jon, as real scientists have hypotheses (not theories) about the early events at and following the origin of life and are actively testing them. 


Isn’t active hypothesis testing the polar opposite of accepting something as axiomatic?

You appear to be projecting your own rejection of the scientific method onto others.

Jon Garvey - #57887

April 13th 2011

“You appear to be projecting your own rejection of the scientific method onto others.”

That may appear to be so but is wrong on two counts (corresponding to the two components of the sentence).

John, it is you who, on another thread, insisted that evolutionary theory must be kept separate from origins of life. Variation and natural selection is only applicable to the DNA code we have, and all work on evolution is done with the existence of that code, and cellular life, as a given. That is the sense in which the natural origin of life and the existence of complex life is axiomnatic.


Hypotheses (and sheer speculations) about the origins of life have been tested for 50 years or more, with singular lack of success. If you accepted, like many other biologists, that information theory applies to DNA then you might well consider that the origin of life had been shown by mathematically demonstrable principles to be unknowable (Yockey, 2005). If that is so, then empirical research in that area is as unscientific as research on negative entropy. If it is not so, then there is still, currently, no scientific basis for preferring one view of OOL over another, including alien or divine origins. It is not, currently, in the realm of science


John - #57952

April 13th 2011

Jon Garvey:

“Variation and natural selection is only applicable to the DNA code we have,…”

False, Jon. Variation and selection are perfectly applicable to RNA as well.

”... and all work on evolution is done with the existence of that code, and cellular life, as a given.”

Again, false. 

“That is the sense in which the natural origin of life and the existence of complex life is axiomnatic.”

Sorry, but since your premises are false, I don’t buy your conclusion.

“Hypotheses (and sheer speculations) about the origins of life have been tested for 50 years or more, with singular lack of success.”

Golly. The 2009 Nobel Prize in Chemistry represents a lack of success to you? Amazing.

“If you accepted, like many other biologists, that information theory applies to DNA then you might well consider that the origin of life had been shown by mathematically demonstrable principles to be unknowable (Yockey, 2005).”

I would call that a hypothesis.

“If that is so, then empirical research in that area is as unscientific as research on negative entropy.”

Then how do YOU explain the nature of peptidyl transferase, Jon? No hearsay, just you.

“If it is not so, then there is still, currently, no scientific basis for preferring one view of OOL over another, including alien or divine origins. It is not, currently, in the realm of science”

You really should start examining evidence for yourself and stop looking only for confirmation.

Mike Gene - #57504

April 9th 2011

Alan,

Sorry for not being clear, Mike. I was wondering if you understood anything by the term, CSI, as it seems impossible for anyone to give any kind of explanation or definition that means anything. As you used CSI in a sentence I was curious as to if you gave the term any credence.

Okay, I see what you are saying.  It has credence in the sense that yes, the receptor is complex, and yes, its ability to bind these ligands is dependent on specific amino acids being in certain positions.  But is that a metric that delivers a design inference?  I think not and Dennis does a nice job of explaining one reason for this. 

How so? By definition, a stochastic event is not predictable (though I see that an apparently random series of chance occurrences  having the “dice loaded” is a way for non-theists and theists to dispense with arguments over intentionality in the scientific realm).

An example of “how so?” was provided in that excerpt from my book:

“A rough analogy to the concept of front-loading is the Las Vegas casino. As long as enough people gamble in the casino, it makes a profit. Yet the profits are derived by people playing games of chance. We cannot predict that a given casino will enjoy a specific profit at a specific time. But we can predict that the casino will profit, because the rules inherent in the games of chance favor the casino. In other words, it is the rules behind the games of chance that front-load profits for the casino.”

Do casinos have to load their die to make a profit?  

A truly clever designer doesn’t need to cheat to bring about a result.  A truly clever designer would know that stochastic events will reliably happen so they can then be exploited by setting them in a context that will  nudge things along particular trajectories.  From this design perspective, stochastic events are fuel, not obstacles.  Take the mutations Dennis writes about above.  Conventional thinking would have us view them as mistakes or errors, as if adaptation was something life resisted.  But I view them as feelers that scan the environment and feedback into the system.



Jon Garvey - #57505

April 9th 2011

Mike, does this not suggest that evolution itself is a selection pressure? There is a selective advantage in changes to the code that mitigate against deleterious effects of mutation and favour the kinds of changes that might well be advantageous.

It’s hard to imagine that a process that has been going on for so long would not in itself be used to advantage, as you suggest (as well as peopke like James Shapiro).


Mike Gene - #57506

April 9th 2011

Hi Jon,

That’s a possibility.  But it’s more than deleterious vs. advantageous.  The system is set up such that there is a huge span of neutral, middle ground.  Think of the deleterious/beneficial mutations as the feelers.  They “connect” the genome to the environment and, in essence, transfer information from the environment back into the genome. But the middle, neutral ground is what makes this system so smart.  Life is able to exploit this middle ground to reposition itself in order to send out new feelers.  It looks like a very well designed system of adaptation that has been able to generate massive diversity upon a deeper theme of massive universality.

Life is not passively shaped by its environment.  It is an active participant in its own evolution.  I talk about one example of this here:
http://designmatrix.wordpress.com/2009/01/20/evolution-under-intrinsic-control/


Jon Garvey - #57511

April 9th 2011

Mike - the link says more or less what I meant, but probably put badly. The paper cited seems more confirmatory evidence for the kind of mechanisms Shapiro suggests. At least in this instance his approach seems similar to yours.

Combine that with the mechanisms in Evo Devo and there’s a whole lot of scope for rapid interesting and innovative species change in response to your local meteorite strike or ice age.

But the really sophisticated ideas in the system seem to go right back to the beginning, which begs the question of how they got there.


Mike Gene - #57614

April 10th 2011

Hi Jon,

Combine that with the mechanisms in Evo Devo and there’s a whole lot of scope for rapid interesting and innovative species change in response to your local meteorite strike or ice age.

Evo-Devo significantly enhances the plausibility of front-loading by more deeply connecting the past to the present (meaning that original designs would remain connected to the future) and showing us that evolution is constrained and, in some way, guided, by the information present in these original states. Consider what biologist Sean Carroll observed:

We now understand that, no, that evolution works with packets of information and uses them in a new and different ways, and new and different combinations, without necessarily having to invent anything fundamentally new, but new combinations.

That evolution works around ancient packets of information and has no need to invent anything fundamentally new is exactly the pattern we would expect from front-loading.

Consider the example Dennis raised.  I would not call it an “example of front-loading,” but it clearly adds to the plausibility of front-loading.  We now have evidence that a receptor protein was able to bind aldosterone 60 million years prior to the appearance of aldosterone.  And this means the affinity for aldosterone was maintained for 60 million years even though there was no selection pressure to specifically maintain aldosterone binding.  A designer with an eye to the future can plan around something like this. Now does this mean such affinity was maintained by some supernatural force? No. Proteins often carry out more than one function and two different functions can be bound through a shared structure (see moonlighting proteins).  It points to proteins as amazing design material, perfectly suited to facilitate evolution.  And if we are smart enough to discover this, a truly smart designer could build their designs around this.

What’s more, the appearance of the two receptors from a single receptor that originally had both functions looks like an example of subfunctionalization mediated by gene duplication, which is also something we would expect from front-loading.  It looks like preadaptation, which is also something we would expect from front-loading.  Like I said, evolution is looking more and more like a splendidly smart process that emerges from the composition and architecture of just two cell plans.  There is no need to impose some non-teleological template on it.  


Arthur Hunt - #57615

April 10th 2011

“A rough analogy to the concept of front-loading is the Las Vegas casino. As long as enough people gamble in the casino, it makes a profit. Yet the profits are derived by people playing games of chance. We cannot predict that a given casino will enjoy a specific profit at a specific time. But we can predict that the casino will profit, because the rules inherent in the games of chance favor the casino. In other words, it is the rules behind the games of chance that front-load profits for the casino.”

Do casinos have to load their die to make a profit?
 


Um, reputable and profitable casinos don’t use loaded die.

The analogy is more insightful than that.

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